The ecological genetics of plant-pathogen interactions in natural communities

Abstract

Plant-fungal pathogen interactions are among the most convenient systems in which to study the full complexity of co-evolved associations. Despite this, the potential ramifications of pathogen-induced damage in plant communities have yet to be widely recognized. Pathogens affect host fitness by reducing fecundity or increasing mortality or both. The consequences of infection by pathogens that have an immediate effect on survival or that totally suppress reproduction are determined relatively easily. However, individual lesions of the type caused by many pathogens are not seriously damaging and their ultimate effect on fitness parameters is often separated temporally from the actual presence of disease symptoms. For annual plants this separation may be relatively short, whereas in perennials both reproduction and survival through periods of stress may be correlated with disease incidence in previous seasons. A causal relation between pathogen-induced reductions in host fitness and demographic and genetic changes in plant populations has yet to be proven. However, circumstantial evidence strongly supports this hypothesis. Natural host populations have often been found to be variable for resistance. Presumably this reflects past selective pressures exerted by the pathogen, but the pattern of the variability can also be influenced by host features such as mating system. Recent work on populations of Glycine spp. (wild soybean) has documented the existence of race specific resistance, which is consistent with the hypothesis that gene-for-gene interactions are an important feature of natural plant-pathogen associations. Pronounced spatial structuring also occurs between closely adjacent populations of both host and pathogen. The major factors which could influence this structuring are small-scale changes in the physical environment, founder effects and localized genetic differentiation in both the host and the pathogen. Models based firmly on realistic ecological and epidemiological assumptions are beginning to provide a picture of the importance of population size and dispersal ability on the stability of natural plant—pathogen interactions.